ArticleScience advances2024
HSP90β controls NLRP3 autoactivation.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- TRIM28 Promotes Keratinocyte Proliferation and Invasion by Activating NLRP3/SGT1 Axis-Mediated Macrophage Pro-Inflammatory Polarization in an In Vitro Macrophage-Keratinocyte Co-Culture Model.Immunity, inflammation and disease · 2026Article
- Disruption of upstream ox-LDL signaling and HSP90-mediated NLRP3 stability protects against experimental steatohepatitis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- HSP90α lactylation orchestrates PGC1α and LRPGC1 nuclear translocation driving mitochondrial biogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- ZNF334 truncation mutation drives cold-induced autoinflammation.EMBO molecular medicine · 2025Article
- DnaJ mediates phage sensing by the bacterial NLR-related protein bNACHT25.PLoS biology · 2025Article
- Implication of the LRR Domain in the Regulation and Activation of the NLRP3 Inflammasome.Cells · 2024Review
- Polydatin-Mediated Inhibition of HSP90α Disrupts NLRP3 Complexes and Alleviates Acute Pancreatitis.Research (Washington, D.C.) · 2024Article
- Mechanisms of Action of HSP110 and Its Cognate Family Members in Carcinogenesis.OncoTargets and therapy · 2024Review
- HSP90 multi-functionality in cancer.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gain-of-function mutations in NLRP3 are linked to cryopyrin-associated periodic syndromes (CAPS). Although NLRP3 autoinflammasome assembly triggers inflammatory cytokine release, its activation mechanisms are not fully understood. Our study used a functional genetic approach to identify regulators of NLRP3 inflammasome formation. We identified the HSP90β-SGT1 chaperone complex as crucial for autoinflammasome activation in CAPS. A deficiency in HSP90β, but not in HSP90α, impaired the formation of ASC specks without affecting the priming and expression of inflammasome components. Conversely, activating NLRP3 with stimuli such as nigericin or alum bypassed the need for SGT1 and HSP90β, suggesting the existence of alternative inflammasome assembly pathways. The role of HSP90β was further demonstrated in PBMCs derived from CAPS patients. In these samples, the pathological constitutive secretion of IL-1β could be suppressed using a pharmacological inhibitor of HSP90β. This finding underscores the potential of SGT1-HSP90β modulation as a therapeutic strategy in CAPS while preserving NLRP3's physiological functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.